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BLOOD CONSERVATION
BRITISH JOURNAL OF ANAESTHESIA
326 that this apparent paradox had to be addressed. We stated that both Libet and Cotterill had proposed that conscious awareness is not necessary for the execution of a simple reaction task. In contrast, we proposed that, in this specific situation (which lies between a conditioned reflex and a voluntary movement), a motor programme might be set up by biasing a set of synapses so that the stimulus automatically triggers the required response. We state that "consciousness is undoubtedly necessary for this programme to be set up and kept in a state of readiness". The later work of Keller and Heckhausen to which Dr Munglani refers is concerned with the initiation of voluntary movements. Whilst this is fascinating in its own right, it is some way from the point of our editorial, which was concerned with conscious awareness. We are sure that Dr Munglani will agree that Libet's work is not familiar to most anaesthetists; nevertheless its wider dissemination will help us to make progress in the difficult problem of understanding and detecting conscious awareness under anaesthesia. J. JESSOP
Doncaster Cambridge
D. W. RYAN D. BELL
Newcastle upon Tyne EUROPEAN STANDARDISATION COMMITTEE ON ANAESTHETIC EQUIPMENT Sir,—As members of the United Kingdom delegation to the European Standardisation Committee on Anaesthetic Equipment CEN/TC215 and its Working Groups, we would like to point out that reference to a private draft committee document made by Dr Zbinden and his colleagues in their article on fresh gas utilization of eight circle systems [1] has not been authorized by the Technical Committee. The test procedure included in the CEN Committee's working document was that proposed by Dr Zbinden's group. It is possible that the proposed fresh gas utilization test will be deleted or changed substantially before publication of the Standard. Some members of the CEN Working Group have expressed doubts about the value of this test in clinical anaesthesia because, as the authors state, the results can be modified greatly by changes in ventilation volume, flow pattern, compliance of the breathing system, leakage, etc. The design and arrangement of components of a circle system to achieve 100% fresh gas utilization would not improve patient safety if the exhaust valve was badly sited, the system resistance high or the leakage excessive. We therefore request that the reference to CEN/TC215/WG1 N36 is not interpreted as providing published international support for this method of apparatus evaluation. R. GREENBAUM
Member of CEN/TC215 B. R. SUGG
Member of CEN/TC215 B. HAYES
Chairman of CEN/TC21S REFERENCE 1. Zbinden AM, Fcigcnwinter, P, Hutmacher M. Fresh gas utilization of eight circle systems. British Journal of Anaesthesia 1991; 67: 492^199.
INCORRECT STATEMENT Sir,—In my article entitled " Indications for Use of Bicarbonate in Patients with Metabolic Acidosis" [1], I stated that THAM is an experimental drug. It is, in fact, approved for use in humans and has been for several years. A. I. ARIEFF
San Francisco REFERENCE 1. Arieff AI. Indications for use of bicarbonate in patients with metabolic acidosis. British Journal of Anaesthesia 1992; 67: 165-177.
REFERENCE 1. Turner DABT. Blood conservation. British Journal of Anaesthesia 1991; 66: 281-284.
MANAGEMENT OF HYPONATRAEMIA Sir,—We read with interest Professor Swales' review on the management of hyponatraemia [1]. However, we should like to draw attention to a situation he has not discussed, namely hyponatraemia caused by natriuresis initiated by intracranial disease. Although relatively rare, this condition is important, as its management differs from that of other causes of hyponatraemia. The term "cerebral salt wasting" was used first in the early 1950s to explain hyponatraemia in patients after subarachnoid haemorrhage (SAH). The cause was thought to be renal sodium loss [2]. However, after the description of the syndrome of inappropriate antidiuretic hormone secretion (SIADH) in 1957, it was assumed widely that water retention was the cause of the (dilutional) hyponatraemia and the term fell into disuse [3]. It was reintroduced in 1981 by Nelson and colleagues, who investigated 12 patients with intracranial pathology who fulfilled established laboratory criteria of SIADH [4]. In 10 of these patients there was a decrease in red cell mass, plasma volume and total blood volume—results which could not be explained by SIADH, as water excess should lead to an expanded circulation in this condition. Natriuresis is a better explanation and cerebral salt wasting a preferable term, as the aetiology is unknown. Cerebral salt wasting has since been reported in many other intracranial pathologies, including disease of the pituitary and its surrounds, head injury and infections including meningitis. Further studies have given support to this concept and atrial natriuretic peptide has been implicated as a possible cause [5-7]. This condition is of more than academic interest, as the treatment of cerebral salt wasting (replace salt and restore circulating volume) is the opposite of fluid restriction used to manage SIADH. Hyponatraemia is common after subarachnoid haemorrhage and recent work indicates that 67 % of these cases are a result of natriuresis and not SIADH [8]. Fluid restriction in any intracranial pathology is potentially dangerous and in SAH increased mortality and morbidity are well documented [9]. Clinicians involved in treating such patients therefore should be aware of this distinction, as inappropriate fluid restriction is hazardous. K. A. SEEX P. R. ELDRIDGE
Liverpool REFERENCES 1. Swales JD. Management of hyponatraemia. British Journal of Anaesthesia 1991; 67: 146-153. 2. Cort JH. Cerebral salt wasting. Lancet 1954; 1: 752-754.
Downloaded from http://bja.oxfordjournals.org/ at Mount Royal University on June 9, 2015
J. G. JONES
BLOOD CONSERVATION Sir,—Dr Turner's editorial on blood conservation [1] dealt with the role of autotransfusion and we wish to comment further. Our experience with the Haemocell 350 system now exceeds 40 patients who have received more than 60 units of salvaged blood. Haemolysis always occurs, but the degree depends on how carefully the surgeon collects salvaged blood, and there is a fast learning curve; it is not clinically significant and does not affect a patient with reasonable renal function. These systems are designed to save red blood cells that would otherwise be discarded, so any cells saved are a bonus. The majority of cells have a perfectly normal survival time. There has been no case of postoperative coagulopathy. Our research indicates that red blood cells passed through a cell washer improve their 2,3-DPG concentrations. Air embolism, loss of platelets and fibrinogen, and microemboli are similar risks to any i.v. transfusions of stored blood. We have been using the system routinely for elective aortic aneurysm, where it makes a beneficial impact on transfusion requirements and gives confidence in using the system in emergency situations.
326 that this apparent paradox had to be addressed. We stated that both Libet and Cotterill had proposed that conscious awareness is not necessary for the execution of a simple reaction task. In contrast, we proposed that, in this specific situation (which lies between a conditioned reflex and a voluntary movement), a motor programme might be set up by biasing a set of synapses so that the stimulus automatically triggers the required response. We state that "consciousness is undoubtedly necessary for this programme to be set up and kept in a state of readiness". The later work of Keller and Heckhausen to which Dr Munglani refers is concerned with the initiation of voluntary movements. Whilst this is fascinating in its own right, it is some way from the point of our editorial, which was concerned with conscious awareness. We are sure that Dr Munglani will agree that Libet's work is not familiar to most anaesthetists; nevertheless its wider dissemination will help us to make progress in the difficult problem of understanding and detecting conscious awareness under anaesthesia. J. JESSOP
Doncaster Cambridge
D. W. RYAN D. BELL
Newcastle upon Tyne EUROPEAN STANDARDISATION COMMITTEE ON ANAESTHETIC EQUIPMENT Sir,—As members of the United Kingdom delegation to the European Standardisation Committee on Anaesthetic Equipment CEN/TC215 and its Working Groups, we would like to point out that reference to a private draft committee document made by Dr Zbinden and his colleagues in their article on fresh gas utilization of eight circle systems [1] has not been authorized by the Technical Committee. The test procedure included in the CEN Committee's working document was that proposed by Dr Zbinden's group. It is possible that the proposed fresh gas utilization test will be deleted or changed substantially before publication of the Standard. Some members of the CEN Working Group have expressed doubts about the value of this test in clinical anaesthesia because, as the authors state, the results can be modified greatly by changes in ventilation volume, flow pattern, compliance of the breathing system, leakage, etc. The design and arrangement of components of a circle system to achieve 100% fresh gas utilization would not improve patient safety if the exhaust valve was badly sited, the system resistance high or the leakage excessive. We therefore request that the reference to CEN/TC215/WG1 N36 is not interpreted as providing published international support for this method of apparatus evaluation. R. GREENBAUM
Member of CEN/TC215 B. R. SUGG
Member of CEN/TC215 B. HAYES
Chairman of CEN/TC21S REFERENCE 1. Zbinden AM, Fcigcnwinter, P, Hutmacher M. Fresh gas utilization of eight circle systems. British Journal of Anaesthesia 1991; 67: 492^199.
INCORRECT STATEMENT Sir,—In my article entitled " Indications for Use of Bicarbonate in Patients with Metabolic Acidosis" [1], I stated that THAM is an experimental drug. It is, in fact, approved for use in humans and has been for several years. A. I. ARIEFF
San Francisco REFERENCE 1. Arieff AI. Indications for use of bicarbonate in patients with metabolic acidosis. British Journal of Anaesthesia 1992; 67: 165-177.
REFERENCE 1. Turner DABT. Blood conservation. British Journal of Anaesthesia 1991; 66: 281-284.
MANAGEMENT OF HYPONATRAEMIA Sir,—We read with interest Professor Swales' review on the management of hyponatraemia [1]. However, we should like to draw attention to a situation he has not discussed, namely hyponatraemia caused by natriuresis initiated by intracranial disease. Although relatively rare, this condition is important, as its management differs from that of other causes of hyponatraemia. The term "cerebral salt wasting" was used first in the early 1950s to explain hyponatraemia in patients after subarachnoid haemorrhage (SAH). The cause was thought to be renal sodium loss [2]. However, after the description of the syndrome of inappropriate antidiuretic hormone secretion (SIADH) in 1957, it was assumed widely that water retention was the cause of the (dilutional) hyponatraemia and the term fell into disuse [3]. It was reintroduced in 1981 by Nelson and colleagues, who investigated 12 patients with intracranial pathology who fulfilled established laboratory criteria of SIADH [4]. In 10 of these patients there was a decrease in red cell mass, plasma volume and total blood volume—results which could not be explained by SIADH, as water excess should lead to an expanded circulation in this condition. Natriuresis is a better explanation and cerebral salt wasting a preferable term, as the aetiology is unknown. Cerebral salt wasting has since been reported in many other intracranial pathologies, including disease of the pituitary and its surrounds, head injury and infections including meningitis. Further studies have given support to this concept and atrial natriuretic peptide has been implicated as a possible cause [5-7]. This condition is of more than academic interest, as the treatment of cerebral salt wasting (replace salt and restore circulating volume) is the opposite of fluid restriction used to manage SIADH. Hyponatraemia is common after subarachnoid haemorrhage and recent work indicates that 67 % of these cases are a result of natriuresis and not SIADH [8]. Fluid restriction in any intracranial pathology is potentially dangerous and in SAH increased mortality and morbidity are well documented [9]. Clinicians involved in treating such patients therefore should be aware of this distinction, as inappropriate fluid restriction is hazardous. K. A. SEEX P. R. ELDRIDGE
Liverpool REFERENCES 1. Swales JD. Management of hyponatraemia. British Journal of Anaesthesia 1991; 67: 146-153. 2. Cort JH. Cerebral salt wasting. Lancet 1954; 1: 752-754.
Downloaded from http://bja.oxfordjournals.org/ at Mount Royal University on June 9, 2015
J. G. JONES
BLOOD CONSERVATION Sir,—Dr Turner's editorial on blood conservation [1] dealt with the role of autotransfusion and we wish to comment further. Our experience with the Haemocell 350 system now exceeds 40 patients who have received more than 60 units of salvaged blood. Haemolysis always occurs, but the degree depends on how carefully the surgeon collects salvaged blood, and there is a fast learning curve; it is not clinically significant and does not affect a patient with reasonable renal function. These systems are designed to save red blood cells that would otherwise be discarded, so any cells saved are a bonus. The majority of cells have a perfectly normal survival time. There has been no case of postoperative coagulopathy. Our research indicates that red blood cells passed through a cell washer improve their 2,3-DPG concentrations. Air embolism, loss of platelets and fibrinogen, and microemboli are similar risks to any i.v. transfusions of stored blood. We have been using the system routinely for elective aortic aneurysm, where it makes a beneficial impact on transfusion requirements and gives confidence in using the system in emergency situations.